How we evolved to trade longevity for vitality

The oldest parts of trees are dead, but the whole keeps on living (Image&colon; Jim Brandenburg/Minden)

Growing old is the price we pay for a vital and productive youth, says Jonathan Silvertown in The Long and Short of It

IN THE Sequoia National Park in central California stands General Sherman, an 80-metre-tall redwood. By the time the tree was discovered in the 19th century – and named after an American Civil War hero to guard against logging – General Sherman was already 2000 years old, a nearly unfathomable age by human standards.

Comparison with paltry human lifetimes might make us wince, but it can also teach us a lot about ourselves, as professor of ecology Jonathan Silvertown explains in The Long and the Short of It, an ideal introduction to the science of ageing and mortality. Interwoven with history and poetry, his erudite and eloquent book concisely explains the mechanisms underlying the lifespan of organisms ranging from nematode worms and chickweed to humans and redwoods. Considering their fates in terms of genetics and environment, Silvertown explores the questions that have bedevilled our species for as long as we’ve had the language to ask&colon; why do we get old and why do we die?

Ageing isn’t a problem for the majestic General Sherman. Senescence – the decline of biological function that we see in ageing – doesn’t really apply to trees. The trunk of a 2000-year-old redwood grows as vigorously as that of a sapling. There’s no decrease in the rate at which new shoots are produced, and the pollen and seeds are still perfectly viable. As Silvertown explains, the key to a tree’s everlasting youth is that it is modular. “All the really old parts of any ancient tree are dead,” he writes. The lifeless central trunk-wood supports the living cambium and branches until structural failure brings down the whole organism.

The modularity of ancient trees provides insight into our own ageing process, argues Silvertown. A tree’s cells divide indefinitely as it continues to grow. Ours are limited by telomeres – caps of non-functional DNA at the ends of chromosomes. These caps protect important genetic code from being cut out during DNA replication but shorten in the process. This reduces the number of times a cell can replicate. This limitation of telomeres provides “a brake that prevents cancer from emerging”, writes Silvertown. Such brakes are unnecessary in trees, because their rigidly modular structures don’t allow cancerous mutations to spread, but for humans telomere-induced “replicative senescence” means cancer cells, too, can have a limited lifetime. As Silvertown explains, it is “the downside experienced in later life of mechanisms that prevent cancer during youth”.

Variations on this theme reverberate throughout Silvertown’s book and throughout life on Earth. Countering the popular notion of ageing and death as analogous to the breakdown of an old machine, he shows how the processes of ageing and death are adaptive trade-offs, negotiated differently by each species in the course of evolution. Reproduction is the essence of genetic survival, individual lifespan be damned.

Ageing and death are adaptive trade-offs, negotiated differently by each species

At the ultimate extreme are organisms such as Pacific salmon, which practise semelparity, dying as soon as they spawn, but there are many far less obvious compromises, such as our susceptibility to autoimmune diseases as we age. Primed to fight off infections between birth and sexual maturity, our immune systems can later drift toward oversensitivity, resulting in diseases such as rheumatoid arthritis, after we’ve fulfilled our reproductive function.

“Natural selection retires in old age,” Silvertown writes, a one-liner with deep scientific and philosophical implications. We’re all semelparous in the end. Death is the price we pay for future generations.